Alcohol ingestion is responsible for the majority of attacks of acute pancreatitis, but the pathogenetic pathways by which this occurs are unknown. Over the past eight years clinical data have been collected that strongly suggest in many alcoholics serum triglyceride elevations caused by the alcohol ingestion initiate the pancreatic inflammation. It has been proposed that free fatty acid release from elevated triglycerides in and around the pancreas and responsible for initiating the pancreatic inflammation. Utilizing an isolated, ex-vivo, perfused canine pancreatic preparation, the various mechanisms by which serum lipid abnormalities might cause pancreatic inflammation will be studied. Respiratory complications in acute pancreatitis are common, but their etiology unknown. The destruction of pulmonary surfactant by circulating pancreatic lecithinase has been proposed as a mechanism by which respiratory failure is initiated. Injury by free fatty acids liberated from elevated serum triglycerides has also been proposed as a pathway by which pulmonary injury might occur. These mechanisms will be evaluated experimentally utilizing an isolated, ex-vivo, perfused, ventilated canine pulmonary lobe. Clinical studies will also be carried out correlating serum lecithinase, free fatty acids, and triglyceride levels in patients with acute pancreatitis, with respiratory status. Finally, since the pathogenesis of acute pancreatitis is unknown, treatment is not based on firm pathophysiology. Atropine administration is fairly routine country-wide, but its efficacy unproven. A prospective clinical trial will be carried out evaluating the effectiveness of atropine in the treatment of acute pancreatitis.